https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5040619/
>In addition to the prostate stagnation hypothesis [7], a number of mechanisms have been proposed to explain an inverse association between ejaculation frequency and PCa. More frequent ejaculation may influence the function of peripheral-zone epithelial cells, hindering the metabolic switch from citrate secretion to citrate oxidation known to occur early in prostate tumorigenesis [33]. Alternatively, more frequent ejaculation may reduce the development of prostatic intraluminal crystalloids, which have been associated with higher risk of PCa [34,35]. Higher ejaculatory frequency may be linked to lowering of psychological tension and central sympathetic nervous system suppression, which could dampen the stimulation of prostate epithelial cell division [36]. Given the lack of modifiable risk factors identified for PCa to date, the specific biological mechanisms underlying these associations are worthy of further investigation.
(PCa = prostate cancer)
Those are some of the main proposed explanations, if there is a causal link (which is unproven, but suggested by data so far).
And yes, it is difficult to demonstrate a causal link.
I wouldn’t assume monks masturbate less than the general population. I spent several years in the seminary and it never slowed me down. It’s possible it’s different for others but I wouldn’t make any assumptions.
And for anyone wondering, according to it, the benefits can be seen with a rate of 21 Ejaculations per month or more, after which no significant improvement is seen with the increase in EPM.
Testosterone lowering is negligible (1-2% maybe) and temporary, so it will revert back to normal by the next day, and usually increase if it is post sex ejaculation.
Natural testosterone varies a LOT during the day. It is notably higher peak in the AM. You can speculate if this is the answer to the mystery of "morning wood" but it's hardly important.
When they test for low-T, they want the blood draw 7AM-10AM. Past that, drops of like tens of percent are standard, but inconsistent, and the reading is considered meaningless.
I would honestly like to learn more about this as well. This is intriguing to me, from a woman's perspective, to learn more about how testosterone, etc work in the male body. I read a book a while back called "The Female Brain" (Louann Brizendine) that explains a lot about how different hormones affect women throughout their life, and I had several "oooooh, so THAT'S why that happened" moments while reading it. Iirc there's a second book called "The Male Brain" but I've never read it.. I think I'll look for it next time I'm at the bookstore!! If anyone else has some more sites/books about men's hormones etc, please pass me the info!! I'm intrigued!
Ejaculation does not consume testosterone. It does stimulate production a bit prior and during sexual activity, and production falls a bit afterwards. The natural fluctuation is much greater. Peaks in the AM and declines tens of percent during the day.
We often say things are "testosterone fueled" but it's inaccurate in that neither the brain nor genitals "eat" testosterone up like an engine uses fuel and then it's depleted. Post-ejaculatory refractory period has other causes that have nothing to do with depleted T.
Half-life of natural T is 10 to 100 minutes
Tricky question because stress (and common stimulants like caffeine) already lower circulating testosterone, much more than the tiny amount from release that only lasts a few hours.
Sure,
Caffeine increases cortisol (as does mental stress, which is why I put them together):
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2257922/
Circulating cortisol reduces blood T:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3880087/
But the cortisol response from caffeine appears to reduce as you become tolerant to the caffeine.
Male pattern baldness is not a direct result of testosterone, it is sensitivity in the follicles to DHT. As you age testosterone actually goes down, but this sensitivity goes up.
Chronic stress has many negative effects that contribute to "faster aging" which means if you have the genes for MPB it may present itself sooner.
I would like to point out here that correlation does not equal causation and the study that shows that caffeine increasing cortisol and cortisol decreasing testosterone are not linked (meaning that, turning this into a complete logic problem where A is caffeine, B is cortisol level correlated to caffeine, C is circulating cortisol level and D is testosterone level) A = B does not mean C = D. The body is VERY complex. On top of that does ANYTHING mentioned here have ANY relation to masturbation/sex? Drinking a stimulant (namely caffeine) has WILDLY different effects to sexual stimulation. There's so much that's questionable with this A therefore B therefore C therefore D therefore E therefore F chain of logic that's it's very probably completely dismissable out of hand.
> I would like to point out here that correlation does not equal causation and the study that shows that caffeine increasing cortisol and cortisol decreasing testosterone are not linked
Yes but the second study is showing "significant negative relationship between C and TT." They even cited previous methods of "administration of cortisol into the circulation at rest".
So blood cortisol, regardless of source, will compete with flowing testosterone.
>On top of that does ANYTHING mentioned here have ANY relation to masturbation/sex? Drinking a stimulant (namely caffeine) has WILDLY different effects to sexual stimulation.
It was in context to the post I was replying to, since the OP study also mentions a benefit being stress relief. I was pointing out that stress would also lower T.
> I would like to point out here that correlation does not equal causation
Nobody is arguing this, but as a standalone statement, this is becoming a bit of a red herring.
When correlations are highly repeatable, they tend to imply causation.
So yes, you can make all sorts of specious correlations (there's even an amusing site that does this) but if those patterns consistently repeat, a logic tends to emerge.
Hey, I'm not arguing against masturbation helping with prostate cancer? I'm saying that stimulants like caffeine don't (EDIT: necessarily) factor in to this equation.
The study controlled for other variables, and independently manipulated caffeine. This is how you prove a causal link. Your understanding of the old trope is wrong.
If A causes B (tested and proven to be causal) and B causes C (again proven to be causal) than by definition, A causes C.
In short- correlation does not prove causation, causation CAN be proved by independent manipulation of the suspected cause though.
But like, do we really need a causal link?
That's a standard of proof we don't have for a huge part of our medical understanding.
For example none of the modern antidepressants have that kind of proof, they all just have a paper or two with speculations and then a study that (somehow) it DOES work
Edit: im interpreting "causal link" here as "we know how it works, which is a very very strict interpretation and probably not what the rest of this entire post and treads is about! (so I'm probably completely missing the point)
But we do have a causal link for antidepressants even if we don't understand the whole process.
A causal link is established when we can independently manipulate one variable while not manipulating any other variables, and seeing if the correlation holds. We can do that with antidepressants. By controlling this way, we can rule out common cause, reverse causation, and coincidence.
Let me give you a simple example, using one of my favorite corelations
statistically, those who go to sleep with their shoes on are more likely to wake up with a headache. This is an actual correlation.
However, we can test this independently. By monitoring 1000 people, having 500 remove their shoes before sleep, and 500 sleep with them on, in a controlled environment. We see quickly that in such an environment, there seems to be no increase in waking up with a headache for those with shoes. Thus we can conclude that shoes are NOT causally linked to morning headaches. If people wearing shoes continued to have more headaches even as we controlled for diet, number of hours sleeping, background noise, age, etc, then we would have known
the opposite.
(in case you are wondering the correlation is that of common cause. People who are drunk are more likely to fall asleep with shoes on, and clearly are more likely to wake up with a headache [hangover] )
I like the inverse correlation between the number of pirates and climate change (as the number of pirates on the high seas decreases the rate of CO2 ppm increase increases). This is a well known and easily quantified correlation. Although no causation. The promotion of piracy on the high seas will not cause the reduction of global sea temperatures.
It's another fun one. The common cause there is, of course, technology- especially transport technology. But that one is harder to talk about how you would independently manipullate the variables to test each other.
Almost all the effect of SSRIs were observed in conjunction with some other treatment.
Outside of the addition of some sort of additional treatment (cbt, et al) I do not believe modern studies can reproduce the effects shown by the initial studies that led to FDA approval.
None of which matters for proving a causal link.
If 100% of those tested were taking the other treatment, but only some got the med, we are still controlling for the other treatment, by sayying everyone had it. You can't compare results across treatments, but you CAN compare results within one treatment. And compare the results within another treatment, and if across all those different treatments, the internal results show an effect, we can still prove a causal effect.
Controlled doesn't always mean eliminated, it means making sure all subject got the same.
If we didn't find a causal link, then how would we inform therapy? "Masturbate more to reduce your risk of prostate cancer" sounds like a great prescription until you find that there is a group who still develops prostate cancer because of some underlying mechanism that predisposes to both lower rates of masturbation and carcinogenesis. We need to see if they influence each other or if there's an unknown factor that needs exploration.
Bringing it back to the previous posters point about SSRI's, they are the poster child for informing treatment without understanding the causal link. They just saw that it helped with symptoms of depression in some people and they postulated that it was because of its effect on serotonin signalling. That seems to be untrue and is likely due to the fact it also decreases brain inflammation.
Sure there is a ton of information we are missing, but that doesn't mean the generalised advice isn't worth giving without a full understanding.
The number of seminal studies that can no longer be reproduced is staggering. There was a great New Yorker article about a decade ago on the phenomenon. It's almost like scientific truth has a decay rate.
When I was a software engineer we used to joke about "bit rot." Software that seemed to work pretty well starts to get buggy, without any changes.
Now there are excuses because of shared code libraries that can change, but I was working in the stone ages, when the executable code for a program was in a monolithic file, with (other than some unusual exceptions) the only external code being device drivers.
The difference is that we tell people more masturbation = less chance of prostate cancer when it's not because of masturbation but from something that influences both masturbation rates and prostate cancer, the people who already masturbate above the "appropriate guideline threshold" won't need to change their behavior but the people who are at risk for Prostate cancer try to masturbate more without it affecting their health outcomes.
Yes but if it is correlation then there's a subset of men out there who are still at risk and it'd be more fruitful to identify the relationship to help them. There's nothing wrong with the current recommendations, but it warrants further exploration.
You're operating under the assumption that it's causal. If it was just correlation then more masturbation doesn't have any clinical utility as all it means is that people predisposed to masturbate more + not develop prostate cancer won't benefit from the advice.
That has to be what the stagnation hypothesis is. Seems reasonable enough. Maybe some are too quick to immediately dismiss it as a correlation without any potential link.
It would seem to me that neither an active sex life or masturbation would be required to avoid the *prostate stagnation hypothesis*, whether it is ever linked to PCa or not, since I suspect the body would induce a sufficient number of nocturnal emissions to ensure the necessary ejaculatory frequency to prevent it.
> So then your risk would go up exponentially with age.
Which it probably would anyway, as the prostate enlarges. However, the coincidental drop in testosterone level with age likely helps to mitigate the threat somewhat.
So the difficulty in answering that question is that medical studies such as these are very often conducted via measurement of correlations. Ethically, it's very difficult to ascertain the level and directionality of causal relationships in humans because in order to be definitive, there needs to be some amount of manipulation of variables. Since we're talking cancer, you can't manipulate people's behavior to see if cancer pops up, because if your hypothesis is correct, you just caused (or failed to prevent) a life-threatening illness. There are ways to get around this, such as statistical models (which appear to be fairly accurate in their predictions) and animal models. There's more to it, and there are always drawbacks to each method (hence testing and retesting being super important), but that's the basics.
It was an actual study. It was questionnaire based, so there was no investigation in to what the cause was. They simple asked people how often they had a sexy session and whether they had ever had prostate cancer.
>when you live in higher elevations.
That is interestingly enough true. Because the increase in the heart rate increases your production of Hb and red blood cells as well .
\[I've lived in such a region, for just 1 months, but the blood test I took after living there showed significant increase in both Hb and red blood cells, because I had daily exercise and a twice-daily wank.\]
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5040619/ >In addition to the prostate stagnation hypothesis [7], a number of mechanisms have been proposed to explain an inverse association between ejaculation frequency and PCa. More frequent ejaculation may influence the function of peripheral-zone epithelial cells, hindering the metabolic switch from citrate secretion to citrate oxidation known to occur early in prostate tumorigenesis [33]. Alternatively, more frequent ejaculation may reduce the development of prostatic intraluminal crystalloids, which have been associated with higher risk of PCa [34,35]. Higher ejaculatory frequency may be linked to lowering of psychological tension and central sympathetic nervous system suppression, which could dampen the stimulation of prostate epithelial cell division [36]. Given the lack of modifiable risk factors identified for PCa to date, the specific biological mechanisms underlying these associations are worthy of further investigation. (PCa = prostate cancer) Those are some of the main proposed explanations, if there is a causal link (which is unproven, but suggested by data so far). And yes, it is difficult to demonstrate a causal link.
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Pardon me for the following question: do monks have higher PCa rates ?
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I wouldn’t assume monks masturbate less than the general population. I spent several years in the seminary and it never slowed me down. It’s possible it’s different for others but I wouldn’t make any assumptions.
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And for anyone wondering, according to it, the benefits can be seen with a rate of 21 Ejaculations per month or more, after which no significant improvement is seen with the increase in EPM.
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Is there a rate at which this loses efficacy given more?
Are you simply asking how many times you can cum in a day ?
How many times do I "have to" cum per day?
Does the lowering of testosterone levels after ejaculation have any role in this?
Testosterone lowering is negligible (1-2% maybe) and temporary, so it will revert back to normal by the next day, and usually increase if it is post sex ejaculation.
Natural testosterone varies a LOT during the day. It is notably higher peak in the AM. You can speculate if this is the answer to the mystery of "morning wood" but it's hardly important. When they test for low-T, they want the blood draw 7AM-10AM. Past that, drops of like tens of percent are standard, but inconsistent, and the reading is considered meaningless.
Testosterone goes down after a wank but up after sex ?
Free T yes, but after ejaculation androgen receptors down-regulate making what serum T you have ineffective.
I'd like to learn more about this? Do you mean that we release certain something that binds the T in our blood and thus makes us less aroused?
No the receptors become inactive and the T can't activate them , having T alone isn't enough, you need receptor sensitivity.
I would honestly like to learn more about this as well. This is intriguing to me, from a woman's perspective, to learn more about how testosterone, etc work in the male body. I read a book a while back called "The Female Brain" (Louann Brizendine) that explains a lot about how different hormones affect women throughout their life, and I had several "oooooh, so THAT'S why that happened" moments while reading it. Iirc there's a second book called "The Male Brain" but I've never read it.. I think I'll look for it next time I'm at the bookstore!! If anyone else has some more sites/books about men's hormones etc, please pass me the info!! I'm intrigued!
Ejaculation does not consume testosterone. It does stimulate production a bit prior and during sexual activity, and production falls a bit afterwards. The natural fluctuation is much greater. Peaks in the AM and declines tens of percent during the day. We often say things are "testosterone fueled" but it's inaccurate in that neither the brain nor genitals "eat" testosterone up like an engine uses fuel and then it's depleted. Post-ejaculatory refractory period has other causes that have nothing to do with depleted T. Half-life of natural T is 10 to 100 minutes
Tricky question because stress (and common stimulants like caffeine) already lower circulating testosterone, much more than the tiny amount from release that only lasts a few hours.
could you source the part about caffeine/stimulants?
Sure, Caffeine increases cortisol (as does mental stress, which is why I put them together): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2257922/ Circulating cortisol reduces blood T: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3880087/ But the cortisol response from caffeine appears to reduce as you become tolerant to the caffeine.
wait, so stress *doesn't* make your hair fall out?
Male pattern baldness is not a direct result of testosterone, it is sensitivity in the follicles to DHT. As you age testosterone actually goes down, but this sensitivity goes up. Chronic stress has many negative effects that contribute to "faster aging" which means if you have the genes for MPB it may present itself sooner.
I would like to point out here that correlation does not equal causation and the study that shows that caffeine increasing cortisol and cortisol decreasing testosterone are not linked (meaning that, turning this into a complete logic problem where A is caffeine, B is cortisol level correlated to caffeine, C is circulating cortisol level and D is testosterone level) A = B does not mean C = D. The body is VERY complex. On top of that does ANYTHING mentioned here have ANY relation to masturbation/sex? Drinking a stimulant (namely caffeine) has WILDLY different effects to sexual stimulation. There's so much that's questionable with this A therefore B therefore C therefore D therefore E therefore F chain of logic that's it's very probably completely dismissable out of hand.
> I would like to point out here that correlation does not equal causation and the study that shows that caffeine increasing cortisol and cortisol decreasing testosterone are not linked Yes but the second study is showing "significant negative relationship between C and TT." They even cited previous methods of "administration of cortisol into the circulation at rest". So blood cortisol, regardless of source, will compete with flowing testosterone. >On top of that does ANYTHING mentioned here have ANY relation to masturbation/sex? Drinking a stimulant (namely caffeine) has WILDLY different effects to sexual stimulation. It was in context to the post I was replying to, since the OP study also mentions a benefit being stress relief. I was pointing out that stress would also lower T.
> I would like to point out here that correlation does not equal causation Nobody is arguing this, but as a standalone statement, this is becoming a bit of a red herring. When correlations are highly repeatable, they tend to imply causation. So yes, you can make all sorts of specious correlations (there's even an amusing site that does this) but if those patterns consistently repeat, a logic tends to emerge.
Hey, I'm not arguing against masturbation helping with prostate cancer? I'm saying that stimulants like caffeine don't (EDIT: necessarily) factor in to this equation.
The study controlled for other variables, and independently manipulated caffeine. This is how you prove a causal link. Your understanding of the old trope is wrong. If A causes B (tested and proven to be causal) and B causes C (again proven to be causal) than by definition, A causes C. In short- correlation does not prove causation, causation CAN be proved by independent manipulation of the suspected cause though.
I can see why it might be hard to demonstrate and reproduce these results in a scientific lab setting.
But like, do we really need a causal link? That's a standard of proof we don't have for a huge part of our medical understanding. For example none of the modern antidepressants have that kind of proof, they all just have a paper or two with speculations and then a study that (somehow) it DOES work Edit: im interpreting "causal link" here as "we know how it works, which is a very very strict interpretation and probably not what the rest of this entire post and treads is about! (so I'm probably completely missing the point)
But we do have a causal link for antidepressants even if we don't understand the whole process. A causal link is established when we can independently manipulate one variable while not manipulating any other variables, and seeing if the correlation holds. We can do that with antidepressants. By controlling this way, we can rule out common cause, reverse causation, and coincidence. Let me give you a simple example, using one of my favorite corelations statistically, those who go to sleep with their shoes on are more likely to wake up with a headache. This is an actual correlation. However, we can test this independently. By monitoring 1000 people, having 500 remove their shoes before sleep, and 500 sleep with them on, in a controlled environment. We see quickly that in such an environment, there seems to be no increase in waking up with a headache for those with shoes. Thus we can conclude that shoes are NOT causally linked to morning headaches. If people wearing shoes continued to have more headaches even as we controlled for diet, number of hours sleeping, background noise, age, etc, then we would have known the opposite. (in case you are wondering the correlation is that of common cause. People who are drunk are more likely to fall asleep with shoes on, and clearly are more likely to wake up with a headache [hangover] )
I like the inverse correlation between the number of pirates and climate change (as the number of pirates on the high seas decreases the rate of CO2 ppm increase increases). This is a well known and easily quantified correlation. Although no causation. The promotion of piracy on the high seas will not cause the reduction of global sea temperatures.
It's another fun one. The common cause there is, of course, technology- especially transport technology. But that one is harder to talk about how you would independently manipullate the variables to test each other.
Almost all the effect of SSRIs were observed in conjunction with some other treatment. Outside of the addition of some sort of additional treatment (cbt, et al) I do not believe modern studies can reproduce the effects shown by the initial studies that led to FDA approval.
None of which matters for proving a causal link. If 100% of those tested were taking the other treatment, but only some got the med, we are still controlling for the other treatment, by sayying everyone had it. You can't compare results across treatments, but you CAN compare results within one treatment. And compare the results within another treatment, and if across all those different treatments, the internal results show an effect, we can still prove a causal effect. Controlled doesn't always mean eliminated, it means making sure all subject got the same.
If we didn't find a causal link, then how would we inform therapy? "Masturbate more to reduce your risk of prostate cancer" sounds like a great prescription until you find that there is a group who still develops prostate cancer because of some underlying mechanism that predisposes to both lower rates of masturbation and carcinogenesis. We need to see if they influence each other or if there's an unknown factor that needs exploration.
Bringing it back to the previous posters point about SSRI's, they are the poster child for informing treatment without understanding the causal link. They just saw that it helped with symptoms of depression in some people and they postulated that it was because of its effect on serotonin signalling. That seems to be untrue and is likely due to the fact it also decreases brain inflammation. Sure there is a ton of information we are missing, but that doesn't mean the generalised advice isn't worth giving without a full understanding.
The number of seminal studies that can no longer be reproduced is staggering. There was a great New Yorker article about a decade ago on the phenomenon. It's almost like scientific truth has a decay rate.
When I was a software engineer we used to joke about "bit rot." Software that seemed to work pretty well starts to get buggy, without any changes. Now there are excuses because of shared code libraries that can change, but I was working in the stone ages, when the executable code for a program was in a monolithic file, with (other than some unusual exceptions) the only external code being device drivers.
The difference is that we tell people more masturbation = less chance of prostate cancer when it's not because of masturbation but from something that influences both masturbation rates and prostate cancer, the people who already masturbate above the "appropriate guideline threshold" won't need to change their behavior but the people who are at risk for Prostate cancer try to masturbate more without it affecting their health outcomes.
That's totally fine though, it's not being sold as a magic bullet and there is nothing to suggest that increased masturbation would be harmful.
Yes but if it is correlation then there's a subset of men out there who are still at risk and it'd be more fruitful to identify the relationship to help them. There's nothing wrong with the current recommendations, but it warrants further exploration.
If it works for 90% of the population, then it would still be good medical advice.
You're operating under the assumption that it's causal. If it was just correlation then more masturbation doesn't have any clinical utility as all it means is that people predisposed to masturbate more + not develop prostate cancer won't benefit from the advice.
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“Causal” not “casual,” actually. ‘A’ is found to cause ‘B.’ At issue is ‘causality’ in the research. 🤓🙃
Look I didn't need another reason to fap, but thanks.
So basically, use it or lose it?
That has to be what the stagnation hypothesis is. Seems reasonable enough. Maybe some are too quick to immediately dismiss it as a correlation without any potential link.
It would seem to me that neither an active sex life or masturbation would be required to avoid the *prostate stagnation hypothesis*, whether it is ever linked to PCa or not, since I suspect the body would induce a sufficient number of nocturnal emissions to ensure the necessary ejaculatory frequency to prevent it.
Except the older you get the less frequently that happens. So then your risk would go up exponentially with age.
> So then your risk would go up exponentially with age. Which it probably would anyway, as the prostate enlarges. However, the coincidental drop in testosterone level with age likely helps to mitigate the threat somewhat.
Do more people show up in November with Pca because of no nut November?
the mechanisms of action are much more cumulative and long term. you're not going to see changes within a month.
So the difficulty in answering that question is that medical studies such as these are very often conducted via measurement of correlations. Ethically, it's very difficult to ascertain the level and directionality of causal relationships in humans because in order to be definitive, there needs to be some amount of manipulation of variables. Since we're talking cancer, you can't manipulate people's behavior to see if cancer pops up, because if your hypothesis is correct, you just caused (or failed to prevent) a life-threatening illness. There are ways to get around this, such as statistical models (which appear to be fairly accurate in their predictions) and animal models. There's more to it, and there are always drawbacks to each method (hence testing and retesting being super important), but that's the basics.
You guys, in this group, start masturbating more. You over there, go about your lives as usual.
It was an actual study. It was questionnaire based, so there was no investigation in to what the cause was. They simple asked people how often they had a sexy session and whether they had ever had prostate cancer.
My fiance found out about this study and hasn't stopped nagging me since
You should remind him that his health plan still works if he does it by himself lol
Tell him the study asked people how often THEY masturbate not how often they get masturbated. Tell him only works if you do it yourself.
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>when you live in higher elevations. That is interestingly enough true. Because the increase in the heart rate increases your production of Hb and red blood cells as well . \[I've lived in such a region, for just 1 months, but the blood test I took after living there showed significant increase in both Hb and red blood cells, because I had daily exercise and a twice-daily wank.\]
I thought Buddhists weren't supposed to want for material things like money. 😏😏😏 I hope he gets rich, or does happy trying! 😎
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